Key result
ACE2 overexpression in transgenic K18-hACE2 mice significantly attenuated progressive cardiac aging phenotypes, including mitochondrial dysfunction and telomere shortening, compared to wild-type controls.
Why the study?
Does ACE2 overexpression protect the heart from aging-induced injury in mice?
Population
Aged C57BL/6 mice and transgenic K18-hACE2 mice
Comparison
Angiotensin-converting enzyme 2 overexpression… vs Wild-type C57BL/6 control mice
Design
Preclinical
Authors
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May support ACE2 modulation for cardiac aging; hypothesis-generating and requires human validation.
Does ACE2 overexpression protect the heart from aging-induced injury in mice?
ACE2 overexpression protects against cardiac aging phenotypes in mice, suggesting it as a potential therapeutic target for anti-aging interventions.
Chen et al. (2026) studied Cardiac aging. ACE2 overexpression (transgenic K18-hACE2 mice) vs. Wild-type controls (C57BL/6 mice) was evaluated on Cardiac aging phenotypes (heart weight, cardiac structure, mitochondrial dysfunction, telomere shortening, immune dysregulation). ACE2 overexpression in transgenic K18-hACE2 mice significantly attenuated progressive cardiac aging phenotypes, including mitochondrial dysfunction and telomere shortening, compared to wild-type controls.